CAJ | 학술논문

目的评价高迁移率族蛋白1 (HMGB1)在内毒素性急性肺损伤大鼠肺血管重构中的作用.方法健康清洁级雄性Wistar大鼠30只,体重220 ～ 250 g,采用随机数字表法,将大鼠随机分为3组(n=10)∶对照组(C组)、内毒素性急性肺损伤模型组(M组)和HMGB1抗体组(H组).C组尾静脉输注生理盐水5 ml/1.5 h;M组输注生理盐水3 ml/1.0h,再输注LPS 2 ml(1 mg/kg)/0.5 h;H组于注射LPS后12、24和36 h时尾静脉注射HMGB1抗体2 mg/kg.于注射LPS后72 h时处死取肺,光镜下观察肺组织病理学结果,采用图像分析软件测量并计算肺小动脉中膜/血管面积百分比,免疫组化法检测肺血管增殖细胞核抗原(PCNA)表达,Western bolt法检测HMGB1表达.结果与C组比较,M组和H组肺小动脉中膜/血管面积百分比、PCNA和HMGB1表达水平升高(P＜0.05),肺组织急性炎症细胞增多,血管壁明显增厚；与M组比较,H组肺小动脉中膜/血管面积百分比、PCNA和HMGB1表达水平降低(P＜0.05),肺组织急性炎症和血管壁增厚明显减轻.结论 HMGB1可能是诱发内毒素性急性肺损伤大鼠肺血管重构的重要因素.
목적 평개고천이솔족단백1 (HMGB1)재내독소성급성폐손상대서폐혈관중구중적작용.방법 건강청길급웅성Wistar대서30지,체중220 ～ 250 g,채용수궤수자표법,장대서수궤분위3조(n=10)∶대조조(C조)、내독소성급성폐손상모형조(M조)화HMGB1항체조(H조).C조미정맥수주생리염수5 ml/1.5 h;M조수주생리염수3 ml/1.0h,재수주LPS 2 ml(1 mg/kg)/0.5 h;H조우주사LPS후12、24화36 h시미정맥주사HMGB1항체2 mg/kg.우주사LPS후72 h시처사취폐,광경하관찰폐조직병이학결과,채용도상분석연건측량병계산폐소동맥중막/혈관면적백분비,면역조화법검측폐혈관증식세포핵항원(PCNA)표체,Western bolt법검측HMGB1표체.결과 여C조비교,M조화H조폐소동맥중막/혈관면적백분비、PCNA화HMGB1표체수평승고(P＜0.05),폐조직급성염증세포증다,혈관벽명현증후；여M조비교,H조폐소동맥중막/혈관면적백분비、PCNA화HMGB1표체수평강저(P＜0.05),폐조직급성염증화혈관벽증후명현감경.결론 HMGB1가능시유발내독소성급성폐손상대서폐혈관중구적중요인소.
Objective To investigate the role of high mobility group protein box 1 (HMGB1) in pulmonary vascular remodeling in a rat model of acute lung injury (ALI).Methods Thirty healthy pathogen free male Wistar rats weighing 220-250 g were randomly divided into 3 groups (n =10 each) ∶ group control (group C) ;group LPS (group M) and group LPS + HMGB1 antibody (group H).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 7 ml/kg.ALI was induced with LPS 1 mg/kg infused iv over 30 min in groups M and H.In group H HMGB1 antibody 2 mg/kg was injected iv at 12,24 and 36 h after LPS administration respectively.The animals were sacrificed at 72 h after LPS administration.The left lung was removed for microscopic examination,measurement of the thickness of the medial layer (tunica media) of pulmonary arterioles and determination of the expression of PCNA (by immune-histochemistry) and HMGB1 protein (by Western blotting).Results The medial layer of pulmonary arterioles was significantly thicker and the expression of PCNA and HMGB1 higher in group M than in group C.LPS also induced significant inflammatory cell infiltration within the alveoli and damage to the septa.In group H HMGB1 antibody significantly attenuated the above-mentioned LPS-induced changes.Conclusion HMGB1 may play an important role in the LPS-induced pulmonary vascular remodeling.